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Titolo:
Human SLPI inactivation after cigarette smoke exposure in a new in vivo model of pulmonary oxidative stress
Autore:
Cavarra, E; Lucattelli, M; Gambelli, F; Bartalesi, B; Fineschi, S; Szarka, A; Giannerini, F; Martorana, PA; Lungarella, G;
Indirizzi:
Univ Siena, Dipartimento Fisiopatol & Med Sperimentale, I-53100 Siena, Italy Univ Siena Siena Italy I-53100 & Med Sperimentale, I-53100 Siena, Italy Semmelweis Univ Med, Dept Med Chem Mol Biol & Pathobiochem, H-1444 Budapest, Hungary Semmelweis Univ Med Budapest Hungary H-1444 em, H-1444 Budapest, Hungary
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 2, volume: 281, anno: 2001,
pagine: L412 - L417
SICI:
1040-0605(200108)281:2<L412:HSIACS>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPITHELIAL PERMEABILITY; N-ACETYLCYSTEINE; RISK-FACTORS; LUNG; RAT; PATHOGENESIS; GLUTATHIONE; EMPHYSEMA; AIRWAYS; DISEASE;
Keywords:
antioxidant status; secretory leukoprotease inhibitor inactivation; bronchoalveolar lavage;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Lungarella, G Univ Siena, Dipartimento Fisiopatol & Med Sperimentale, Via Aldo Moro, I-53100 Siena, Italy Univ Siena Via Aldo Moro Siena Italy I-53100 0 Siena, Italy
Citazione:
E. Cavarra et al., "Human SLPI inactivation after cigarette smoke exposure in a new in vivo model of pulmonary oxidative stress", AM J P-LUNG, 281(2), 2001, pp. L412-L417

Abstract

The role of oxidative stress in inactivating antiproteases is the object of debate. To address this question, we developed an in vivo model of pulmonary oxidative stress induced by cigarette smoke (CS) in mice. The major mouse trypsin inhibitor contrapsin is not sensitive to oxidation, and the mouse secretory leukoprotease inhibitor (SLPI) does not inhibit trypsin. Instead, human recombinant (hr) SLPI inhibits trypsin and is sensitive to oxidation. Thus we determined the effect of CS in vivo on hrSLPI antiproteolytic function in the airways of mice. CS caused a significant decrease in total antioxidant capacity in bronchoalveolar lavage fluid (BALF) and significant changes in oxidized glutathione, ascorbic acid, protein thiols, and 8-epi-PGF2(alpha). Intratracheal hrSLPI significantly increased BALF antitryptic activity. CS induced a 50% drop in the inhibitory activity of hrSLPI. Pretreatment with N-acetylcysteine prevented the CS-induced loss of hrSLPI activity, the decrease in antioxidant defenses, and the elevation of 8-epi-PGF-2 alpha. Thus an inactivation of hrSLPI was demonstrated in this model. This is a novel model for studying in vivo the effects of CS oxidative stress onhuman protease inhibitors with antitrypsin activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 02:52:02